ReviewCellular and molecular life sciences : CMLS2026
ERKed by too much signaling: from oncogenic driver to therapeutic vulnerability.
Review in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
5 authors.
Funding
Abstract
Extracellular regulated kinase (ERK) signaling is a major driver of cancer development. Mutations accumulated in oncogenes upstream of ERK can promote and sustain tumorigenesis by providing a sustained proliferative signal, helping cells resist death, and inducing angiogenesis. Therapeutic strategies for cancers with dysregulated ERK signaling have focused on inhibiting upstream-mutated oncogenes as a means of depriving tumors of these essential survival cues. While these strategies have demonstrated initial clinical success in patients, they also represent an incomplete understanding of the more nuanced role ERK signaling plays in tumor cell homeostasis. It is now understood that increased ERK signaling can also function as a tumor suppressor by inducing proliferative arrest outside of the framework of oncogene-induced senescence. In this review, we highlight current research describing the vulnerability of cancer cells to ERK hyperactivation induced toxicity and offer insight on how ERK rewiring may be leveraged for the development of new therapeutic strategies for patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.